Current Osteoporosis Reports最新文献

Purpose of review: There is strong evidence that poor dietary intake of certain micro- and macro-nutrients can negatively affect bone health. It is unclear if diet is the primary culprit for poor bone health in the vegan population.

Recent findings: Plant-based diets are gaining public interest since they may improve metabolic health. Studies that examine vegetarians and vegans together show a lower bone mineral density (BMD), but not always increased fracture risk compared to omnivores. However, vegans consistently have higher risk of fracture at multiple bone sites, especially at the hip. There is higher fracture risk in vegans which may be due to calcium and vitamin D intake, as well as amount of dietary protein and quality. Other nutrients (B vitamins, Se, Zn, Fe, iodine) or physiological factors (lower body mass index, microbiome, or endocrine profile) may also play a role but have not been examined and require further study.

Purpose of review: Osteocytes are the most abundant cell type in bone. These unique cells act primarily as mechanosensors and play crucial roles in the functional adaptation of bone tissue. This review aims to summarize the recent microfluidic studies on mechanically stimulated osteocytes in regulating other cell types.

Recent findings: Microfluidics is a powerful technology that has been widely employed in recent years. With the advantages of microfluidic platforms, researchers can mimic multicellular environments and integrate dynamic systems to study osteocyte regulation under mechanical stimulation. Microfluidic platforms have been developed to investigate mechanically stimulated osteocytes in the direct regulation of multiple cell types, including osteoclasts, osteoblasts, and cancer cells, and in the indirect regulation of cancer cells via endothelial cells. Overall, these microfluidic studies foster the development of treatment approaches targeting osteocytes under mechanical stimulation.

Purpose of review: To revisit the bone tissue mechanotransduction mechanisms behind the bone tissue response to mechanical loading and, within this context, explore the possible negative influence of regular swimming practice on bone health, particularly during the growth and development period.

Recent findings: Bone is a dynamic tissue, responsive to mechanical loading and unloading, being these adaptative responses more intense during the growth and development period. Cross-sectional studies usually report a lower bone mass in swimmers compared to athletes engaged in weigh-bearing sports. However, studies with animal models show contradictory findings about the effect of swimming on bone health, highlighting the need for longitudinal studies. Due to its microgravity characteristics, swimming seems to impair bone mass, but mostly at the lower limbs. It is unkown if there is a causal relationship between swimming and low BMD or if other confounding factors, such as a natural selection whithin the sport, are the cause.

Purpose of review: Diabetes mellitus is defined by elevated blood glucose levels caused by changes in glucose metabolism and, according to its pathogenesis, is classified into type 1 (T1DM) and type 2 (T2DM) diabetes mellitus. Diabetes mellitus is associated with multiple degenerative processes, including structural alterations of the bone and increased fracture risk. High-resolution peripheral computed tomography (HR-pQCT) is a clinically applicable, volumetric imaging technique that unveils bone microarchitecture in vivo. Numerous studies have used HR-pQCT to assess volumetric bone mineral density and microarchitecture in patients with diabetes, including characteristics of trabecular (e.g. number, thickness and separation) and cortical bone (e.g. thickness and porosity). However, study results are heterogeneous given different imaging regions and diverse patient cohorts.

Recent findings: This meta-analysis assessed T1DM- and T2DM-associated characteristics of bone microarchitecture measured in human populations in vivo reported in PubMed- and Embase-listed publications from inception (2005) to November 2021. The final dataset contained twelve studies with 516 participants with T2DM and 3067 controls and four studies with 227 participants with T1DM and 405 controls. While T1DM was associated with adverse trabecular characteristics, T2DM was primarily associated with adverse cortical characteristics. These adverse effects were more severe at the radius than the load-bearing tibia, indicating increased mechanical loading may compensate for deleterious bone microarchitecture changes and supporting mechanoregulation of bone fragility in diabetes mellitus. Our meta-analysis revealed distinct predilection sites of bone structure aberrations in T1DM and T2DM, which provide a foundation for the development of animal models of skeletal fragility in diabetes and may explain the uncertainty of predicting bone fragility in diabetic patients using current clinical algorithms.

Purpose of review: To provide an overview of the recent literature investigating the pathophysiology of skeletal muscle changes, interventions for skeletal muscle, and effects of exercise in chronic kidney disease (CKD).

Recent findings: There are multiple CKD-related changes that negatively impact muscle size and function. However, the variability in the assessment of muscle size, in particular, hinders the ability to truly understand the impact it may have in CKD. Exercise interventions to improve muscle size and function demonstrate inconsistent responses that warrant further investigation to optimize exercise prescription. Despite progress in the field, there are many gaps in the knowledge of the pathophysiology of sarcopenia of CKD. Identifying these gaps will help in the design of interventions that can be tested to target muscle loss and its consequences such as impaired mobility, falls, and poor quality of life in patients with CKD.

Purpose of review: This review summarizes recent developments on the effects of glycemic control and diabetes on bone health. We discuss the foundational cellular mechanisms through which diabetes and impaired glucose control impact bone biology, and how these processes contribute to bone fragility in diabetes.

Recent findings: Glucose is important for osteoblast differentiation and energy consumption of mature osteoblasts. The role of insulin is less clear, but insulin receptor deletion in mouse osteoblasts reduces bone formation. Epidemiologically, type 1 (T1D) and type 2 diabetes (T2D) associate with increased fracture risk, which is greater among people with T1D. Accumulation of cortical bone micro-pores, micro-vascular complications, and AGEs likely contribute to diabetes-related bone fragility. The effects of youth-onset T2D on peak bone mass attainment and subsequent skeletal fragility are of particular concern. Further research is needed to understand the effects of hyperglycemia on skeletal health through the lifecycle, including the related factors of inflammation and microvascular damage.

Purpose of review: The purpose of this review is to discuss the molecular mechanisms involved in osteocyte dendrite formation, summarize the similarities between osteocytic and neuronal projections, and highlight the importance of osteocyte dendrite maintenance in human skeletal disease.

Recent findings: It is suggested that there is a causal relationship between the loss of osteocyte dendrites and the increased osteocyte apoptosis during conditions including aging, microdamage, and skeletal disease. A few mechanisms are proposed to control dendrite formation and outgrowth, such as via the regulation of actin polymerization dynamics. This review addresses the impact of osteocyte dendrites in bone health and disease. Recent advances in multi-omics, in vivo and in vitro models, and microscopy-based imaging have provided novel approaches to reveal the underlying mechanisms that regulate dendrite development. Future therapeutic approaches are needed to target the process of osteocyte dendrite formation.

Purpose of review: The purpose of the review is to summarize the expression and function of CSF1R and its ligands in bone homeostasis and constraints on therapeutic targeting of this axis.

Recent findings: Bone development and homeostasis depends upon interactions between mesenchymal cells and cells of the mononuclear phagocyte lineage (MPS), macrophages, and osteoclasts (OCL). The homeostatic interaction is mediated in part by the systemic and local production of growth factors, macrophage colony-stimulating factor (CSF1), and interleukin 34 (IL34) that interact with a receptor (CSF1R) expressed exclusively by MPS cells and their progenitors. Loss-of-function mutations in CSF1 or CSF1R lead to loss of OCL and macrophages and dysregulation of postnatal bone development. MPS cells continuously degrade CSF1R ligands via receptor-mediated endocytosis. As a consequence, any local or systemic increase or decrease in macrophage or OCL abundance is rapidly reversible. In principle, both CSF1R agonists and antagonists have potential in bone regenerative medicine but their evaluation in disease models and therapeutic application needs to carefully consider the intrinsic feedback control of MPS biology.

Purpose of review: To summarise the current evidence and clinical practices for patients with fragility fractures of the pelvis (FFP).

Recent findings: FFPs are an increasingly prevalent and recognised problem in the elderly population. Recent evidence indicates they have a significant impact on function, morbidity and mortality. While traditional management of FFPs was predominantly non-surgical, surgical options have been increasingly used, with a range of surgical methods available. To date, limited consensus exists on the optimal strategy for suitable patient selection, and clinical trials in this population have proved problematic. The management of FFPs requires a multi-faceted approach to enhance patient care, including adequate pain control, minimisation of complications and optimisation of medical management. Early return to mobilisation should be a key treatment goal to maintain functional independence. The selection of patients who will maximally benefit from surgical treatment, and the most appropriate surgical strategy to employ, remains contentious.

Purpose of review: This review aims to summarize the recent findings about the contribution of the gut microbiome to muscle pathophysiology and discuss molecular pathways that may be involved in such process. Related findings in the context of cancer cachexia are outlined.

Recent findings: Many bacterial metabolites have been reported to exert a beneficial or detrimental impact on muscle physiology. Most of the evidence concentrates on short-chain fatty acids (SCFAs), with an emerging role for bile acids, bacterial amino acid metabolites (bAAms), and bacterial polyphenol metabolites. Other molecular players worth considering include cytokines, hormones, lipopolysaccharides, and quorum sensing molecules. The current literature clearly establishes the ability for the gut microbiome to modulate muscle function and mass. The understanding of the mechanisms underlying this gut-muscle axis may lead to the delivery of novel therapeutic tools to tackle muscle wasting in cancer cachexia, chronic kidney disease, liver fibrosis, and age-related sarcopenia.